[Hyperphosphatemia and cardiovascular diseases : impact of vascular calcification and endothelial dysfunction].

Hyperphosphatemia has clinically been associated with total mortality and cardiovascular mortality in patients with chronic renal failure (CRF). Recently, higher serum phosphate levels within the normal range have been shown to be associated with substantially increased risk of cardiovascular events even in patients without CRF. Therefore, it is clear that the phosphate axis may in fact play a role in atherogenesis. Accumulating mechanistic studies regarding local effects of phosphate on the vessel wall have recently provided insight into various pathways that culminate in vascular smooth muscle cell (SMC) calcification. SMC phenotypic change into osteochondrogenic differentiation and SMC apoptosis are essential roles in hyperphosphatemia-induced vascular calcification. In addition, Hyperphosphatemia induces endothelial dysfunction via various mechanisms, including a decline in nitric oxide release due to oxidative stress. The sodium-dependent phosphate cotransporter PiT-1 is required for these effects. This review shows the current knowledge about phosphate-induced changes in the vascular wall, leading to atherosis and sclerosis.